In 1917, the War Department’s star medical team knew what to expect. Proud of their expertise and the status of the medical profession, they resolved that infectious diseases would not decimate the AEF. No shrinking violet, Dr. Vaughan reeled off facts with the calm authority of a medical school dean. “The mobilization of an army is a medical as well as a military problem,” he warned army brass. “[Making] raw, untrained men…into effective soldiers [has] always been accompanied by marked increase in morbidity [sickness] and mortality.” Crowd diseases could turn training camps into “drag-nets” for infections.21
Science had already helped bring under control some of the diseases that had devastated armies in the past. By 1918, the U.S. army was vaccinating recruits against smallpox, cholera, typhoid fever, and anthrax. Vaughan suggested other sensible measures: more Medical Corps doctors, more hospitals, more nutritious food, less crowding in barracks, better sanitation. The army should assemble newly drafted recruits into groups of not more than thirty near their homes. There they would be examined, vaccinated, bathed, scrubbed, issued clean uniforms, and isolated for two weeks, long enough for symptoms of any disease they might have to show up.22
U.S. soldiers line up to receive typhoid fever vaccinations during World War I. (1917) Credit 30
Officers responsible for training the AEF had different concerns. Armies, they declared, existed to win wars. “The purpose of mobilization,” Vaughan and his colleagues were told, “is to convert civilians into trained soldiers as quickly as possible and not to make a demonstration in preventive medicine.” Translation: You may give any advice you wish, but remember that the military has a job to do, and that job comes first.23
A sentence in the army’s official medical manual fairly leaped off the page. It said that the prime concern of military physicians was the “preservation of the strength of the Army in the field.” It followed, as one officer put it, that “from a cold military standpoint the care of the well and strong is more important than the care of the ill and feeble.” War is a taskmaster; it demands hard, often cruel, choices. Nothing could be worse than losing a war; such a loss could threaten the nation’s very existence. So “a patient’s interests” had to yield to “the stern activities of war.”24
Professional medical judgment, therefore, was at odds with the necessities of waging war. In peacetime, the physician’s duty was to preserve the health of any individual who needed help. But in the war’s big picture, an individual doughboy’s life counted for little; his loss was merely “wastage,” an inevitable cost of carrying out a mission. Similarly, the physician was bound not only by professional standards but also by the patriotic duty to prepare recruits to fight for “the greater good,” as defined by a democratically elected government. Frustrating as these facts were, a different challenge soon revealed a critical gap in physicians’ knowledge: they knew nothing about viruses.25
OF BACTERIA AND VIRUSES
In 1918, when physicians used the term virus, derived from the Latin for “a poisonous force,” they meant toxins (poisons) given off by bacteria. No less an authority than Sir William Osler (1849–1919), the leading English physician of the day, spoke of the “virus of anthrax,” a bacterial disease attacking plant-eating animals. Osler had no idea that viruses are separate entities, unlike bacteria in every way. To understand the difference, we must base our discussion on research done in the decades after World War I.26
Physicians already knew a lot about how bacteria looked and behaved. Bacteria are single-celled organisms. We call them organisms because they do everything necessary for life. They take in and digest food, use energy to grow and develop, and eliminate waste. Bacteria reproduce by growing to twice their normal size and then splitting into two “daughter” cells, each exact copies of the “parent.” Bacteria can divide about once every twenty minutes. At that rate, a single bacterium may produce four sextillion (the number 4 followed by twenty-one zeros) copies of itself.27
All living cells, from the single cell of a bacterium to the billions of cells that make up a human being, contain strands of a material called deoxyribonucleic acid—DNA for short. Joined in a double helix, these strands resemble a spiral staircase. DNA is the chemical instruction manual for how living organisms look and function. Segments of DNA strands called genes control heredity, the passing of physical qualities from parent to offspring.
The double-stranded helix of DNA. Credit 31
Bacteria are the oldest known lifeforms. Microscopic fossils reveal they have been around for at least 3.5 billion years. Fossils also show that they attacked Tyrannosaurus rex, a huge flesh-eating dinosaur that roamed the earth 65 million years ago. Scientists have found living bacteria in every environment: water, soil, clouds, hot springs, volcanic vents, Arctic ice, and the oceans’ depths. What is more, bacteria live on and in the human body: our skin, hair, nose, mouth, teeth, eyelids, stomach, intestines, and lungs. Amazingly, we have ten times as many bacterial cells in our bodies as human cells. As biologist Thomas Borody jokingly put it, “We are 10 percent human, 90 percent poo.”28
Bacteria cause diseases such as bubonic plague, typhoid fever, typhus, tuberculosis, cholera, diphtheria, and whooping cough. They enter our bodies with the air we inhale, in the water we drink and the food we eat, through breaks in our skin, during sexual activity. However, less than 1 percent of the thousands of known types of bacteria make us sick. Most are usually harmless and often helpful. Life could not exist on Earth without these tiniest of organisms. Bacteria produce about half the oxygen in our planet’s atmosphere. Some types purify water in sewage-treatment plants; some break down oil spills. Still others act as nature’s waste-disposal crews, dissolving dead animals and plants. Many life-forms need the chemicals bacteria leave behind to survive. Bacteria, too, help our bodies digest food and produce vitamins K and B12, both essential to health.29
Viruses are much simpler things. We call them “things” because they are merely bundles of genetic material enclosed in a protein envelope called a capsule. Their genes are either double-stranded DNA or single strands of ribonucleic acid—RNA for short. Nobel Prize–winning biologist Peter Medawar defined the virus as “a piece of bad news wrapped up in protein.” Viruses are bad news. Throughout the ages, they have caused dreadful diseases: measles, mumps, polio, chicken pox, smallpox, hepatitis, rabies, Ebola, AIDS, and influenza, to name a few.30
Virologists—scientists who study viruses—have identified and described about 5,000 types, though they suspect a million others may exist. Viruses are found wherever there are living cells to invade. Their numbers are astounding, more than all earthly creatures combined. Science writer Carl Zimmer estimates there are about a nonillion (the number 1 followed by thirty zeros) viruses in the oceans alone. Were you to put all of them on a scale, they would equal the weight of seventy-five million blue whales, the largest living creatures.31
Yet viruses are tiny, about 1/10,000th of a millimeter; a billion could fit onto the head of a pin. Viruses can pass through the finest filters and are invisible under ordinary microscopes. Many virologists say viruses exist on the edge of life, somewhere between a living organism and a pure chemical. They do not consider them to be alive, because viruses have no working parts—unlike bacteria, they can do nothing on their own.
For a virus to harm humans, six things need to happen: (1) The virus must emerge from the animal that shelters its kind. (2) It must be spread easily by its human host—through coughing, sneezing, touching, kissing, or sexual activity. (3) It must enter human cells quickly, because it cannot exist for long outside its host. (4) Once inside a host, it needs to evade a savage hunter, the human immune system. (5) It has to hijack living cells, forcing them to make more of its own kind. (6) The next generation of the virus must spread from person to person; if it cannot, its type will disappear.
Viruses seem to exist for one purpose only: to reproduce. Nevertheless, they cannot divide like bacteria or have sex like animals. Yet viruses are fussy;
different types zero in on specific types of cells but not on other types. A target cell may be a bacterium of a certain kind, or the target cell may be one of the specialized cells that make up the tissues and organs of complex creatures like ourselves.
Let’s say a certain type of virus targets epithelial cells—tissue that lines the skin, mouth, intestines, etc. After finding its prey, the virus attaches itself to the cell wall, gradually forcing its way inside. Once inside, the virus sheds its protein envelope and releases its DNA or RNA genes (it cannot have both) into the nucleus, which is the cell’s command-and-control center. As if ordering the nucleus, “Stop what you are doing and obey me!” the invading genes reprogram the cell’s genes to make copies of the virus. The cell has no choice; it must become the invader’s slave. Now unable to tend to its own needs, the cell can only manufacture copies of the virus. Before long, the cell fills with “newborn” viruses until it can hold no more. At that point, the viruses burst through the wall, killing the weakened cell, and go on to infect nearby cells of the same kind. As the infection spreads, either the host creature dies or its immune system fights off the infection. No other outcome is possible.
Our immune system ranks high among Mother Nature’s marvels. Its job is to distinguish “self ” from “nonself”—that is, the body’s own cells from the cells of invaders. When a bacterium or a virus enters our body, chemicals called cytokines (from Greek words meaning “cell movement”) detect the intruder immediately. Saying, in effect, “You are not of me,” the chemicals send out signals to trigger the body’s defenses. The first sign of trouble is fever, the body’s way of “baking” intruders to death.
Meanwhile, more aid rushes to the infected site. Key aid givers are two types of white blood cells known as leukocytes. The first type, called phagocytes, surrounds intruders and gobbles them up. The second type, called lymphocytes, consists of B cells and T cells. Both types patrol the body, always ready for action. B cells make antibodies, chemicals that destroy intruders or neutralize the toxins they produce. T cells have more to do. Some destroy the body’s own infected cells. Others serve as “memory cells,” allowing the immune system to respond quickly to a later invasion by the same or a similar intruder. This is the principle of vaccination: memory cells recognize past intruders, jolting the immune system into action without causing a full-blown infection.
Today, we use the term virus for not only natural viruses but also manmade ones. A computer virus is a program that gets into your computer, usually from an infected website or an email attachment. Once inside, it forces your computer to make as many copies of itself as possible, as quickly as possible. This, in turn, uses up all the computer’s memory, disabling the machine by making its operating system “freeze”—come to a halt. Viruses can also spread across networks, infecting every computer linked to them. However, various security programs “immunize” computers, preventing viruses from entering, or removing them when they do.
THE DEVIL VIRUS
The influenza virus is unique. Science historian John Barry says it is “among the most perfect” of viruses. What makes it so is its ability to change continually; it never stays the same. This cannot be said about other viruses. For instance, the virus that causes polio (infantile paralysis) is very stable, so the same vaccine will give immunity year after year. And if injected before symptoms develop, the rabies vaccine will prevent the disease in a person bitten by any rabid, or “mad,” animal.32
There are three forms of the influenza virus: Type A, Type B, and Type C. Type C can make humans seriously ill, but it seldom does. Type B is more annoying than dangerous. Type A can become a mass killer. Moreover, humans, whales, horses, pigs, dogs, cats, apes, baboons, walruses, and seals have their own special versions of the Type A virus.33
All flu viruses that make humans sick get their start in birds. Wild birds that live in water, especially ducks and geese, are their natural “reservoirs.” These viruses live in the birds’ intestines. Apparently, over millions of years, waterbirds and viruses adjusted to this arrangement; they do not harm each other. Humans, however, usually do not get influenza directly from birds. Even when they do, the virus rarely spreads from person to person. For the virus to be able to attack humans, it must first pass through pigs.
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Flu viruses may actually drop from the sky. Imagine a flock of wild ducks migrating, flying thousands of miles to winter nesting grounds. As they pass overhead, some drop feces, which happen to land in pigpens. Not surprisingly, bits of the virus-laden stuff get into the animals’ nostrils. The danger lies in some pigs already having two versions of the Type A virus in their bodies: their own and the version from their human handlers. In that case, pig lung cells become “mixing vessels” for bird, pig, and human viral genes.
Mixing works like this: The capsule of the Type A virus is studded with spikes made of two kinds of proteins, known as H and N, shorthand for hemagglutinin and neuraminidase. Scientists have assigned these proteins numbers based on their appearance. The Type A H1N1 virus was the culprit in the 1918 pandemic. Its H-protein spikes act as grappling hooks to attach the virus to the outer wall of a cell in the throat or lungs before penetrating it. After forcing the host cell to produce more viruses, the new generation’s H-protein spikes go into action. Each spike has four propeller-like blades, which slice through the cell’s inner wall, freeing the “newborn” viruses. When this happens, between 100,000 and a million viruses literally explode through the cell wall at once.34
Influenza viruses have eight genes made of RNA. These differ in a special way from the genes of viruses made of DNA. Each DNA gene has a built-in checking mechanism that scans for copying errors in “newborn” viruses. When these errors are found, a DNA gene can either repair itself or self-destruct. Genes made of RNA lack this self-scanning ability, so the copying errors common in flu genes cannot be fixed or eliminated. To further complicate matters, the genes of flu viruses, unlike the genes of most other viruses, are not aligned to form a single strand. Instead, they come in separate segments. Though “newborn” viruses still have eight genes, their separate segments allow the genes of birds, humans, and pigs to arrange themselves at random within the same host cell. Virologists call this process reassortment. The result of reassortment is a genetic mutation, an aspect that the original virus lacks but its later versions can inherit.
Reassorted Type A bird and pig flu genes enable the virus to move from pig to pig, producing deadly “swine flu.” Reassortments of bird and human flu genes allow infection to cross over to people and then from one person to another. Highly contagious, the recombined virus spreads by droplets expelled by coughing and sneezing. A hearty sneeze sends upward of 40,000 virus particles hurtling through the air at a speed of 152 feet per second. Influenza viruses can travel up to twelve feet, and they are so light that they can remain suspended in the air for up to thirty minutes. To become infected, a person has to inhale only one of the suspended viruses. Infection can also come from touching a surface on which a suspended virus has landed. This makes influenza an ideal crowd disease.35
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Most mutations are not extreme. Virologists say viruses drift—that is, each generation undergoes a series of small changes. But these “newborn” viruses remain much like the “parent” generation. The similarity is still close enough to allow the human immune system’s memory cells to recognize the intruder and mount a defense. Over time, however, mutations accumulate, making it harder to detect later generations of intruders. That is why we need to get an updated version of the flu vaccine every year.
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Influenza viruses can also mutate suddenly and dramatically. When this happens, scientists say they shift, giving rise to a completely new form of the virus. If this form has a feature that improves its chances to reproduce, such as an enhanced ability to clamp on to a cell wall, it will cause trouble. Because the human immune system has never before encountered such an intruder, it cannot recogn
ize the threat at first, or act to destroy it quickly. What is worse, as a new virus generation passes from person to person, it strengthens with each passage, having gained fresh opportunities for mutation. For example, we now know that the devil virus of 1918 did not start out as a mass killer. But as the infection spread, the virus shifted, becoming deadlier. At the same time, the war acted as an accelerator, creating conditions that allowed the mutated virus to explode into a pandemic that killed tens of millions.
THE FIRST WAVE
Morale in the Allied countries had reached a low point by the fall of 1917. “The war [is] eating into the souls of men,” British and French people murmured. A young Londoner told her diary: “[Everywhere] there is an all-pervading atmosphere of dread.”36
There was plenty of reason to worry. A four-month campaign in Belgium had cost the British army 250,000 lives and achieved absolutely nothing. In the east, meanwhile, the Russians, who had been suffering crushing defeats, saw revolutionaries topple their government. Almost immediately, they found themselves in a savage civil war. Reds (Communists) and Whites (those loyal to the old monarchy) butchered each other without mercy. Unable to fight a civil war and Germany at the same time, the Reds begged for peace. Germany agreed, and on December 2, 1917, Russia left the war, a major setback for the Allies.
Very, Very, Very Dreadful Page 5